Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1982-7-8
pubmed:abstractText
The effects of a panel of H-2Kb mutants on the presentation of the non-H-2 histocompatibility (H) antigens H-4.2 and H-3.1 to antigen-specific T cells were examined. Kb-restricted cytotoxic effector T cells were presented with H-4.2 and H-3.1 in the context of mutant Kb alleles. H-4.2 was differentially presented by Kb mutants to Kb-restricted cytotoxic effectors. Cold target inhibition analysis demonstrated that Kb-restricted, H-4.2-specific cytotoxic effectors recognized H-4.2 in the context of at least three restriction sites on the Kb molecule. One site is specific for Kb alone, whereas two additional sites are differentially expressed by Kb mutant molecules. The effect of Kb mutations on the presentation of H-4.2 and H-3.1 was H antigen-specific. Identical, respective patterns of presentation of H-4.2 and H-3.1 by Kb mutants were observed with Kb-restricted T cells proliferating in secondary mixed lymphocyte culture. Further, individual mice varied in their preference for H-3.1 presented in the context of different Kb mutant molecules. These observations demonstrate that the presentation of H antigens by mutant Kb molecules is antigen-specific; analysis of presentation of H antigen by mutants to wild-type Kb-restricted effectors allows the identification of multiple restriction sites on the Kb molecule.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:volume
128
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2629-33
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1982
pubmed:articleTitle
H-2 effects on cell-cell interactions in the response to single non-H-2 alloantigens. V. Effects of H-2Kb mutations on presentation of H-4 and H-3 alloantigens.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.